>>BNTA

BNTA

Catalog No.GC60650

강력한 세포외 기질(ECM) 조절제인 BNTA는 SOD3(초산화물 디스뮤타제 3)를 활성화하여 연골 세포에서 연골 구조 분자 합성을 촉진합니다.

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BNTA Chemical Structure

Cas No.: 685119-25-9

Size 가격 재고 수량
5mg
US$278.00
재고 있음
10mg
US$464.00
재고 있음
25mg
US$881.00
재고 있음
50mg
US$1,437.00
재고 있음

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Sample solution is provided at 25 µL, 10mM.

Description Chemical Properties Product Documents Related Products

BNTA, a potent extracellular matrix (ECM) modulator, facilitates cartilage structural molecule synthesis on chondrocytes by activating superoxide dismutase 3 (SOD3). BNTA promotes cartilage extracellular matrix generation and inhibits osteoarthritis development. BNTA has the potential for the research of osteoarthritis[1].

BNTA (0.01-10 μM; 1-7 d) does not decrease cell viability of human osteoarthritis chondrocytes and rat primary chondrocytes[1].BNTA (0.1 μM; 2 d) increases SOX9 protein markedly[1].BNTA (0.1 μM; 2 d) remarkably increases the COL2A1 and SOX9 protein levels in IL1β-induced rat OA chondrocytes[1].BNTA (10 μM; 5 d) increases proteoglycan staining in ATDC5 cells[1].BNTA (0.01-10 μM; 6 h) upregulates the expression levels of ECM-related genes COL2A1, ACAN, proteoglycan 4 (PRG4), and SRY-box 9 (SOX9) in human OA chondrocytes[1].BNTA (0.01-10 μM; 6 h) increases Col2a1, Acan, Prg4, and Sox9 mRNA levels, with maximum effects around 0.1 μM in IL1β-induced rat OA chondrocytes[1].BNTA (0.01-1 μM; 2 or 3 w) enhances anabolism and inhibited inflammatory response in osteoarthritis cartilage explants[1]. Cell Viability Assay[1] Cell Line: Human OA chondrocytes

BNTA (0.015-1.5 mg/kg; intra-articular injection; twice a week for 4 and 8 weeks) could attenuate OA progression developed after anterior cruciate ligament transection (ACLT) in rats[1]. Animal Model: Male SD rats weighing 80 g are induced by ACLT[1]

[1]. Shi Y, et, al. A small molecule promotes cartilage extracellular matrix generation and inhibits osteoarthritis development. Nat Commun. 2019 Apr 23; 10(1): 1914.

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Average Rating: 5 ★★★★★ (Based on Reviews and 27 reference(s) in Google Scholar.)

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